Ectopic expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4ppk.PG causes a robust presynaptic terminal overgrowth and significantly increases the number of connectives in class IV dendritic arborizing neurons in third instar larvae compared to controls.
Expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in embryos results in fuzzy commissures, a defect caused by extra axons crossing the midline.
Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4insc-Mz1407 causes multiple Fas2-positive axon bundles to ectopically cross the midline in most segments of nearly all embryos examined.
Stage 16 embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS driven by Scer\GAL4ftz.ng display axon bundles that cross the midline inappropriately.
Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, causes a strong increase in axonal extension and arborization of the sLNv.
Limiting expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS to primarily pCC/MP2 neurons using Scer\GAL4ftz.ng is sufficient to induce on average three to four Fas2-positive axons to cross the midline incorrectly in all embryos examined.
Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4elav.PLu results in axonal midline-crossing abnormalities.
Embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL431 have defects in the central nervous system (CNS); the longitudinal and commissural axons are less tightly bundled than normal and increased numbers of axons exit the CNS from the longitudinal tracts. Flies expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4hs.2sev are viable and fertile and have a severe rough eye phenotype; the eyes are small and bar-shaped with a large reduction in the number of ommatidial facets. The facets are abnormally shaped and vary in size. Multiple misplaced mechanosensory bristles and lens defects are seen. The ommatidia lack one or more retinal cells and/or have elongated or fused rhabdomeres or retinal cells. The secondary and tertiary pigment cells are disorganised.
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by fraΔP1.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by fraΔP2.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by fra3/fra[+]
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by fra3/fra4/fraUAS.cKa, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by fraΔP1.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-enhanceable by fra3/fra4/fraΔP2.UAS, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has abnormal neuroanatomy | embryonic stage 16 phenotype, non-enhanceable by fraΔP3.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by fraΔP3.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, suppressible by fra3/fra4
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by fra3/fra[+]
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by fra3/fra4/fraUAS.cKa, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by fraΔP1.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by fra3/fra4/fraΔP2.UAS, Scer\GAL4insc-Mz1407
Scer\GAL4insc-Mz1407/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of fra3/fra4
Abl::Hsap\ABL1::Hsap\BCRP210.UAS/Scer\GAL4ftz.ng is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of robo11
Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is an enhancer of abnormal neuroanatomy | embryonic stage 16 | dominant phenotype of sli1
Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is a suppressor of abnormal neuroanatomy phenotype of comm1
Abl::Hsap\ABL1::Hsap\BCRP210.UAS/Scer\GAL4ftz.ng is a suppressor of abnormal neuroanatomy phenotype of comm1
Scer\GAL431/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is a suppressor of lethal phenotype of Abl1/Df(3L)st-j7
Scer\GAL431/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is a suppressor | partially of lethal phenotype of Abl1/Df(3L)st-j7, NrtM2
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1, Scer\GAL431 has viable phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1, Scer\GAL431 has visible phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, Scer\GAL431 has visible phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has visible phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by fraUAS.cKa, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by fraΔP1.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by fraΔP1.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, enhanceable by fraΔP2.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, enhanceable by fraΔP2.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, non-enhanceable by fra3/fra[+]
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, non-enhanceable by fra3/fra4/fraUAS.cKa, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, non-enhanceable by fraΔP1.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, non-enhanceable by fra3/fra4/fraΔP2.UAS, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has larval ventral nerve cord commissure | embryonic stage 16 phenotype, non-enhanceable by fraΔP3.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4ftz.ng has commissure | embryonic stage 16 phenotype, non-enhanceable by fraΔP3.UAS, Scer\GAL4ftz.ng
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has commissure | ectopic phenotype, suppressible | partially by fraΔP3.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has commissure | ectopic phenotype, suppressible by fra3/fra4
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, non-suppressible by fra3/fra[+]
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has commissure | ectopic phenotype, non-suppressible by fra3/fra4/fraUAS.cKa, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has commissure | ectopic phenotype, non-suppressible by fraΔP1.UAS/fra3/fra4, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407 has commissure | ectopic phenotype, non-suppressible by fra3/fra4/fraΔP2.UAS, Scer\GAL4insc-Mz1407
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4P2.4.Pdf has ventral adult lateral neuron & axon phenotype, non-suppressible by Appld
Scer\GAL4insc-Mz1407/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is an enhancer of larval ventral nerve cord commissure phenotype of fra3/fra4
Abl::Hsap\ABL1::Hsap\BCRP210.UAS/Scer\GAL4ftz.ng is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo11
Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is an enhancer of larval longitudinal connective | embryonic stage 16 phenotype of sli1
Abl::Hsap\ABL1::Hsap\BCRP210.UAS/Scer\GAL4ftz.ng is a suppressor of symmetrical commissure phenotype of comm1
Scer\GAL4elav.PLu/Abl::Hsap\ABL1::Hsap\BCRP210.UAS is a suppressor of symmetrical commissure phenotype of comm1
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Scer\GAL4insc-Mz1407, fra3/fra4 has tract | ectopic | embryonic stage phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, Scer\GAL431 has eye phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, Scer\GAL431 has ommatidium phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has eye phenotype
Abl::Hsap\ABL1::Hsap\BCRP210.UAS, Abl1/Df(3L)st-j7, NrtM2, Scer\GAL431 has ommatidium phenotype
The lethality of Abl1/Df(3L)st-j7 is rescued by Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS expressed under the control of Scer\GAL431. The rescued flies are variably fertile and have rough eyes. The lethality of Abl1/NrtM2 Df(3L)st-j7 is partially rescued by Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS expressed under the control of Scer\GAL431. The rescued flies are fertile and have rough eyes.
Over-expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4insc-Mz1407 enhances the degree of thinning and missing posterior commissures in fra3/fra4 embryos, and many anterior commissures disappear. Large bundles of axons are observed ectopically exiting the central nervous system (CNS), often extending beyond the CNS/PNS boundary. The anterior commissures, which are virtually unaffected in fra3/fra4 embryos, are thin or missing in 41% of segments.
Fuzzy commissures remain evident in heterozygous fra3 embryos expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4insc-Mz1407.
Re-expression of fraScer\UAS.cKa in fra3/fra4 mutants reverts the phenotype back to that seen when Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is expressed alone under the control of Scer\GAL4insc-Mz1407 : fuzzy commissures.
In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP1.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.
In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP2.Scer\UAS is able tor revert the commissure loss seen in fra3/fra4 mutants. These mutants display fuzzy commissures.
In fra3/fra4 mutants expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, expression of fraΔP3.Scer\UAS restores commissure formation in fra3/fra4 mutants. The frequency of fuzzy commissures is also significantly reduced.
fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS.
fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraScer\UAS.cKa is co-expressed.
fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP1.Scer\UAS is co-expressed.
fra3/fra4 fails to reduce the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP2.Scer\UAS is co-expressed.
fra3/fra4 significantly reduces the frequency of ectopic axonal midline-crossovers resulting from the expression of Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS when fraΔP3.Scer\UAS is co-expressed.
Nearly a third of hemi-segments in fra3/fra4 embryos expressing Scer\GAL4insc-Mz1407>Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS exhibit defects characterised by Fas2-positive axons ectopically exiting the central nervous system (CNS).
The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is significantly increased by co-expression of fraScer\UAS.cKa.
The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is significantly increased by co-expression of fraΔP1.Scer\UAS.
The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is significantly increased by co-expression of fraΔP2.Scer\UAS.
The frequency of neuronal crossover projections induced by Scer\GAL4ftz.ng-driven expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS is not significantly increased by co-expression of fraΔP3.Scer\UAS.
Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS, under the control of Scer\GAL4P2.4.Pdf, in a Appld background still induces the axonal arborization phenotype that occurs when the transgene is expressed in a wild-type background.
Compared with heterozygous robo1 mutants alone, expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS using Scer\GAL4ftz.ng enhances the frequency of abnormal axonal crossovers. Almost every segment of every robo1/+ embryo expressing Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS exhibits abnormal crossovers.
Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in heterozygous sli1 mutants results in a collapse of the longitudinal connectives towards the midline.
Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.
Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in a subset of neurons under the control of Scer\GAL4ftz.ng partially suppresses the comm1 commissure phenotype.
The part of the chimeric construct derived from human sequences corresponds to the P210 BCR-ABL1 fusion protein found in chronic myelogenous leukemia.